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VWF (von Willebrand Factor) Is Not Required for Red Blood Cell Retention in Clots in Mice

VWF (von Willebrand Factor) Is Not Required for Red Blood Cell Retention in Clots in Mice Arteriosclerosis, Thrombosis, and Vascular Biology RESEARCH LETTER VWF (von Willebrand Factor) Is Not Required for Red Blood Cell Retention in Clots in Mice Lori A. Holle , Dougald M. Monroe , Alisa S. Wolberg enous thrombosis and pulmonary embolism (collec- To investigate the contribution of VWF to RBC reten- tively venous thromboembolism) affect 1 to 2/1000 tion in clots, we collected blood from 18 to 22 week Vpeople annually. Venous thromboembolism has old wild-type (4 male, 3 female) or VWF-deficient ≈30% mortality, usually associated with pulmonary (B6.129S2-Vwf [tm1Wgr], 9 male, 4 female) C57BL6/J embolism and is the third leading cause of cardiovascu- mice (The Jackson Laboratory, Bar Harbor, ME) via infe- rior vena cava puncture into 3.2% sodium citrate (10% lar death worldwide. v/v, final). Data from males and females were not differ- Venous thrombosis is initiated by blood stasis and ent and were pooled for each genotype. Hematocrit was activation of coagulation, resulting in intravascular throm- similar between groups (39.2±1.1 versus 40.4±1.7%, bin generation and fibrin deposition. Trapping of red VWF-sufficient versus -deficient blood, respectively). We blood cells (RBCs) within the fibrin network and platelet- recalcified blood and triggered clotting with tissue factor mediated contraction of the thrombus http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis, Thrombosis & Vascular Biology Wolters Kluwer Health

VWF (von Willebrand Factor) Is Not Required for Red Blood Cell Retention in Clots in Mice

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References (6)

Publisher
Wolters Kluwer Health
Copyright
© 2020 American Heart Association, Inc.
ISSN
1079-5642
eISSN
1524-4636
DOI
10.1161/ATVBAHA.120.314575
Publisher site
See Article on Publisher Site

Abstract

Arteriosclerosis, Thrombosis, and Vascular Biology RESEARCH LETTER VWF (von Willebrand Factor) Is Not Required for Red Blood Cell Retention in Clots in Mice Lori A. Holle , Dougald M. Monroe , Alisa S. Wolberg enous thrombosis and pulmonary embolism (collec- To investigate the contribution of VWF to RBC reten- tively venous thromboembolism) affect 1 to 2/1000 tion in clots, we collected blood from 18 to 22 week Vpeople annually. Venous thromboembolism has old wild-type (4 male, 3 female) or VWF-deficient ≈30% mortality, usually associated with pulmonary (B6.129S2-Vwf [tm1Wgr], 9 male, 4 female) C57BL6/J embolism and is the third leading cause of cardiovascu- mice (The Jackson Laboratory, Bar Harbor, ME) via infe- rior vena cava puncture into 3.2% sodium citrate (10% lar death worldwide. v/v, final). Data from males and females were not differ- Venous thrombosis is initiated by blood stasis and ent and were pooled for each genotype. Hematocrit was activation of coagulation, resulting in intravascular throm- similar between groups (39.2±1.1 versus 40.4±1.7%, bin generation and fibrin deposition. Trapping of red VWF-sufficient versus -deficient blood, respectively). We blood cells (RBCs) within the fibrin network and platelet- recalcified blood and triggered clotting with tissue factor mediated contraction of the thrombus

Journal

Arteriosclerosis, Thrombosis & Vascular BiologyWolters Kluwer Health

Published: Aug 25, 2020

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